The DOI matches its Crossref record; 149 of the 149 references it cites were found in a registry or an index.
Molecular mechanisms of renal aging
Open accessAbstract
Epidemiologic, clinical, and molecular evidence suggest that aging is a major contributor to the increasing incidence of acute kidney injury and chronic kidney disease. The aging kidney undergoes complex changes that predispose to renal pathology. The underlying molecular mechanisms could be the target of therapeutic strategies in the future. Here, we summarize recent insight into cellular and molecular processes that have been shown to contribute to the renal aging phenotype.The main clinical finding of renal aging is the decrease in glomerular filtration rate, and its structural correlate is the loss of functioning nephrons. Mechanistically, this has been linked to different processes, such as podocyte hypertrophy, glomerulosclerosis, tubular atrophy, and gradual microvascular rarefaction. Renal functional recovery after an episode of acute kidney injury is significantly worse in elderly patients. This decreased regenerative potential, which is a hallmark of the aging process, may be caused by cellular senescence. Accumulation of senescent cells could explain insufficient repair and functional loss, a view that has been strengthened by recent studies showing that removal of senescent cells results in attenuation of renal aging. Other potential mechanisms are alterations in autophagy as an important component of a disturbed renal stress response and functional differences in the inflammatory system. Promising therapeutic measures to counteract these age-related problems include mimetics of caloric restriction, pharmacologic renin-angiotensin-aldosterone system inhibition, and novel strategies of senotherapy with the goal of reducing the number of senescent cells to decrease aging-related disease in the kidney.
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“As individuals age, the kidneys undergo various structural impairments, such as fibrosis, and experience functional issues, including mitochondrial dysfunction (Fig. 3).144–146”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [146]
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Cites
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
Dimri, G. P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens, M., Rubelj, I., & Pereira-Smith, O. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.20.9363 · Cited by 7,477
The limited in vitro lifetime of human diploid cell strains
Hayflick, L. (1965) · Experimental Cell Research · doi:10.1016/0014-4827(65)90211-9 · Cited by 5,876
Telomeres shorten during ageing of human fibroblasts
Harley, C. B., Futcher, A. B., & Greider, C. W. (1990) · Nature · doi:10.1038/345458a0 · Cited by 5,750
The retinoblastoma protein and cell cycle control
Weinberg, R. A. (1995) · Cell · doi:10.1016/0092-8674(95)90385-2 · Cited by 4,862
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., van de Sluis, B., Kirkland, J. L., & van Deursen, J. M. (2011) · Nature · doi:10.1038/nature10600 · Cited by 3,670
Empagliflozin and Progression of Kidney Disease in Type 2 Diabetes
Wanner, C., Inzucchi, S. E., Lachin, J. M., Fitchett, D., von Eynatten, M., Mattheus, M., Johansen, O. E., Woerle, H. J., Broedl, U. C., & Zinman, B. (2016) · New England Journal of Medicine · doi:10.1056/nejmoa1515920 · Cited by 3,655
Aging, Cellular Senescence, and Cancer
Campisi, J. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183653 · Cited by 2,954 · cited 1×
“Active p53 is able to initiate either apoptosis or senescence via transcriptional upregulation of proapoptotic genes or the cyclin-dependent kinase inhibitor p21CIP1/WAF1, the latter of which inhibits cyclindependent kinases that inactivate the retinoblastoma protein.(52) Hypophosphorylation of the retinoblastoma”
BackgroundNaturally occurring p16Ink4a-positive cells shorten healthy lifespan
Baker, D. J., Childs, B. G., Durik, M., Wijers, M. E., Sieben, C. J., Zhong, J., A. Saltness, R., Jeganathan, K. B., Verzosa, G. C., Pezeshki, A., et al. (2016) · Nature · doi:10.1038/nature16932 · Cited by 2,876
The role of senescent cells in ageing
van Deursen, J. M. (2014) · Nature · doi:10.1038/nature13193 · Cited by 2,623
Cellular senescence in aging and age-related disease: from mechanisms to therapy
Childs, B. G., Durik, M., Baker, D. J., & van Deursen, J. M. (2015) · Nature Medicine · doi:10.1038/nm.4000 · Cited by 2,363
Cited by
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Inflammation and aging: signaling pathways and intervention therapies
Li, X., Li, C., Zhang, W., Wang, Y., Qian, P., & Huang, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01502-8 · Cited by 1,443
Bao, H., Cao, J., Chen, M., Min, C., Chen, W., Chen, X., Chen, Y., Chen, Y., Chen, Y., Chen, Z., et al. (2023) · Science China Life Sciences · doi:10.1007/s11427-023-2305-0 · Cited by 392
Chen, L., Yang, T., Lu, D., Zhao, H., Feng, Y., Chen, H., Chen, D., Vaziri, N. D., & Zhao, Y. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.02.090 · Cited by 363
Sirt3-mediated mitophagy regulates AGEs-induced BMSCs senescence and senile osteoporosis
Guo, Y., Jia, X., Cui, Y., Song, Y., Wang, S., Geng, Y., Li, R., Gao, W., & Fu, D. (2021) · Redox Biology · doi:10.1016/j.redox.2021.101915 · Cited by 299
Immune cells and inflammation in AKI to CKD progression
Sato, Y., & Yanagita, M. (2018) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00195.2018 · Cited by 273
“Functional and structural impairment in aged kidneys as well as chronic inflammatory traits contribute to increased risk for AKI to CKD progression and developing AKI in the elderly (37, 121, 142).”
Background
Metadata
- Authors
- Schmitt, R., & Melk, A.
- Affiliations
- Medizinische Hochschule Hannover (DE)
- Venue
- Kidney International
- Publisher
- Elsevier BV
- Published
- 2017-09
- Volume
- 92
- Issue
- 3
- Pages
- 569-579
- ISSN
- 0085-2538 (ISSN-L)
- OpenAlex
- W2737090018
- Cited by
- 235
- References
- 149
- Citations by year
- 2026: 18 · 2025: 27 · 2024: 31 · 2023: 32 · 2022: 30 · 2021: 32 · 2020: 29 · 2019: 19 · 2018: 15 · 2017: 2
- FWCI
- 2.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Kidney International (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
- Keywords
- kidney aging, acute kidney injury, chronic kidney disease, glomerular filtration rate decline, nephron loss, podocyte hypertrophy, glomerulosclerosis, tubular atrophy, microvascular rarefaction, cellular senescence, senolytics, autophagy, renal inflammation, caloric restriction mimetics, renin-angiotensin-aldosterone system inhibition, kidney regeneration
- MeSH terms
- Aging, Angiotensin-Converting Enzyme Inhibitors, Animals, Autophagy, Disease Models, Animal, Disease Susceptibility, Glomerular Filtration Rate, Humans, Kidney, Renin-Angiotensin System, Cellular Senescence, Caloric Restriction, Acute Kidney Injury
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